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Growing evidence suggests an independent relationship between habitual snoring and metabolic abnormalities. Currently, there are few data available on the association between snoring and hyperuricemia. Therefore, we evaluated the cross-sectional association between snoring and serum uric acid (UA) concentration and ascertain the effects of different snoring intensities on hyperuricemia among Chinese urban adults in Nanjing.We performed a cross-sectional study including 7699 participants (4197 men and 3502 women) from Nanjing Drum Tower Hospital aged ≥18 years over a two year (ie, 2016-2018) period. All participants were divided into four groups based on Snoring scores. Questionnaires, physical examinations and biochemical tests were conducted. Hyperuricemia was defined as levels of serum UA6.8 mg/dL in males and6.0 mg/dL in females. We used a generalized linear model to investigate the association between snoring and serum UA concentration and logistic regression model to investigate the association between snoring and likelihood of having hyperuricemia in the age-, sex-adjusted model and in a multivariable model adjusting for demographic factor, plasma lipid profiles, blood glucose, blood pressure, smoking, and alcohol consumption.The prevalence of hyperuricemia was 10.05% in the studied population and gradually increased across the snoring scores (P 0.0001). We found that mild snoring, moderate, and severe snoring intensity were associated with high serum UA in the age-, sex-adjusted model and in a multivariable model adjusting for demographic and lifestyle/behavioral risk factors. The association was insisted with the addition of variables related to clinical outcomes such as diabetes, hypertension, and high-cholesterol levels.Our results showed self-reported habitual snoring was associated with higher serum UA concentration among Chinese urban adults. Findings of this study indicate the significance of early detection and treatment of snoring to prevent hyperuricemia.

The global rise in obesity has become a public health crisis. During the onset of obesity, disrupted catecholamine signals have been described to contribute to excess fat accumulation, however, the molecular and metabolic change of subcutaneous adipose tissue (SAT) upon chronic high-fat feeding has rarely been investigated. Here, we show that chronic high-fat feeding caused a significant decrease in the expression of thermogenic genes and acquisition of partial deleterious features of visceral fat in SAT. Upregulated miR-149-3p was involved in this obesity-induced “visceralization” of SAT via inhibiting PRDM16, a master regulator that promoted SAT thermogenesis. Reduction of miR-149-3p significantly increased PRDM16 expression in SAT, with improved whole-body insulin sensitivity, decreased SAT inflammation, and liver steatosis in high-fat fed mice. These findings provided direct evidence of the anti-obese and anti-diabetic effect of PRDM16 in the obese background for the first time and identified that miR-149-3p could serve as a therapeutic target to protect against diet-induced obesity and metabolic dysfunctions. Keywords: diet-induced obesity, miR-149-3p, Prdm16, subcutaneous adipose tissue, thermogenesis